31,077 research outputs found
A model for gene deregulation detection using expression data
In tumoral cells, gene regulation mechanisms are severely altered, and these
modifications in the regulations may be characteristic of different subtypes of
cancer. However, these alterations do not necessarily induce differential
expressions between the subtypes. To answer this question, we propose a
statistical methodology to identify the misregulated genes given a reference
network and gene expression data. Our model is based on a regulatory process in
which all genes are allowed to be deregulated. We derive an EM algorithm where
the hidden variables correspond to the status (under/over/normally expressed)
of the genes and where the E-step is solved thanks to a message passing
algorithm. Our procedure provides posterior probabilities of deregulation in a
given sample for each gene. We assess the performance of our method by
numerical experiments on simulations and on a bladder cancer data set
A transfer-learning approach to feature extraction from cancer transcriptomes with deep autoencoders
Publicado en Lecture Notes in Computer Science.The diagnosis and prognosis of cancer are among the more
challenging tasks that oncology medicine deals with. With the main aim
of fitting the more appropriate treatments, current personalized medicine
focuses on using data from heterogeneous sources to estimate the evolu-
tion of a given disease for the particular case of a certain patient. In recent
years, next-generation sequencing data have boosted cancer prediction by
supplying gene-expression information that has allowed diverse machine
learning algorithms to supply valuable solutions to the problem of cancer
subtype classification, which has surely contributed to better estimation
of patient’s response to diverse treatments. However, the efficacy of these
models is seriously affected by the existing imbalance between the high
dimensionality of the gene expression feature sets and the number of sam-
ples available for a particular cancer type. To counteract what is known
as the curse of dimensionality, feature selection and extraction methods
have been traditionally applied to reduce the number of input variables
present in gene expression datasets. Although these techniques work by
scaling down the input feature space, the prediction performance of tradi-
tional machine learning pipelines using these feature reduction strategies
remains moderate. In this work, we propose the use of the Pan-Cancer
dataset to pre-train deep autoencoder architectures on a subset com-
posed of thousands of gene expression samples of very diverse tumor
types. The resulting architectures are subsequently fine-tuned on a col-
lection of specific breast cancer samples. This transfer-learning approach
aims at combining supervised and unsupervised deep learning models
with traditional machine learning classification algorithms to tackle the
problem of breast tumor intrinsic-subtype classification.Universidad de Málaga. Campus de Excelencia Internacional AndalucÃa Tech
Joint Structure Learning of Multiple Non-Exchangeable Networks
Several methods have recently been developed for joint structure learning of
multiple (related) graphical models or networks. These methods treat individual
networks as exchangeable, such that each pair of networks are equally
encouraged to have similar structures. However, in many practical applications,
exchangeability in this sense may not hold, as some pairs of networks may be
more closely related than others, for example due to group and sub-group
structure in the data. Here we present a novel Bayesian formulation that
generalises joint structure learning beyond the exchangeable case. In addition
to a general framework for joint learning, we (i) provide a novel default prior
over the joint structure space that requires no user input; (ii) allow for
latent networks; (iii) give an efficient, exact algorithm for the case of time
series data and dynamic Bayesian networks. We present empirical results on
non-exchangeable populations, including a real data example from biology, where
cell-line-specific networks are related according to genomic features.Comment: To appear in Proceedings of the Seventeenth International Conference
on Artificial Intelligence and Statistics (AISTATS
Causality, Information and Biological Computation: An algorithmic software approach to life, disease and the immune system
Biology has taken strong steps towards becoming a computer science aiming at
reprogramming nature after the realisation that nature herself has reprogrammed
organisms by harnessing the power of natural selection and the digital
prescriptive nature of replicating DNA. Here we further unpack ideas related to
computability, algorithmic information theory and software engineering, in the
context of the extent to which biology can be (re)programmed, and with how we
may go about doing so in a more systematic way with all the tools and concepts
offered by theoretical computer science in a translation exercise from
computing to molecular biology and back. These concepts provide a means to a
hierarchical organization thereby blurring previously clear-cut lines between
concepts like matter and life, or between tumour types that are otherwise taken
as different and may not have however a different cause. This does not diminish
the properties of life or make its components and functions less interesting.
On the contrary, this approach makes for a more encompassing and integrated
view of nature, one that subsumes observer and observed within the same system,
and can generate new perspectives and tools with which to view complex diseases
like cancer, approaching them afresh from a software-engineering viewpoint that
casts evolution in the role of programmer, cells as computing machines, DNA and
genes as instructions and computer programs, viruses as hacking devices, the
immune system as a software debugging tool, and diseases as an
information-theoretic battlefield where all these forces deploy. We show how
information theory and algorithmic programming may explain fundamental
mechanisms of life and death.Comment: 30 pages, 8 figures. Invited chapter contribution to Information and
Causality: From Matter to Life. Sara I. Walker, Paul C.W. Davies and George
Ellis (eds.), Cambridge University Pres
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